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A solid phase radioimmunoassay (RIA) was used to detect Aspergillus antigenemia in three patients, two with autopsy proved disseminated aspergillosis and one with a suspected infection. These RIA studies suggest that screening for antigenemia may be a specific and sensitive diagnostic test for disseminated aspergillosis.
Invasive aspergillosis generally occurs in patients with hematologic malignancies, neutropenia or other severe derangements of host defense. An adult patient without such a predisposition, and without a previous history of susceptibility to infections, had rapidly progressive respiratory failure associated with repeated growth of Aspergillus fumigatus on culture of sputum and bronchoscopy specimens. At autopsy he proved to have invasive pulmonary aspergillosis.
Locally invasive aspergillosis of the bowel and peritoneal cavity is a rare complication of immunosuppression, broad-spectrum antibiotic therapy, and corticosteroid administration. We present the case of a 9-year-old boy with acute lymphocytic leukemia who presented with a small bowel obstruction. Surgical treatment of the aspergillosis required multiple aggressive resections of all involved bowel segments. Parenteral nutrition and intravenous Amphotericin B and 5-Fluorocytosine therapy were also instituted. Achievement of a hematologic remission is another prerequisite for cure.
Aspergillosis of the central nervous system is rare. The spread to the CNS is usually from the lungs and uncommonly from paranasal sinuses. Four cases of CNS aspergillosis with spread of infection from the paranasal sinuses are described. Two patients had meningitis, one intracranial granuloma and one presented with subarachnoid haemorrhage resulting from a fungal mycotic aneurysm. Difficulties in establishing the diagnosis are discussed.
Aspergillosis of the paranasal sinuses is an infrequently reported disease which can occur in two forms: (1) a noninvasive form that can clinically mimic nonspecific chronic sinusitis and (2) an invasive form that can simulate malignant disease of the sinuses. The disease occurs without known predisposing systemic disease. Primary treatment consists of surgical eradication of infected tissue. The question of whether concomitant antifungal chemotherapy should be used in the noninvasive form of aspergillosis has not been definitely resolved. Presented is a review of the literature, the report of a case, and a discussion of possible pathogenic mechanisms.
Antral aspergillosis has recently been found to be often induced by endodontic material (Endomethasone, N2, Riebler Material), that contains zinc oxide and paraformaldehyde. A study of 34 otherwise healthy patients with aspergillus infection of the maxillary sinus had a pathognomonic radiologic appearance noted in 26 patients (76%). All patients except one had a history of endodontic therapy. The radiology, pathogenesis, differential diagnosis, treatment, and prevention of solitary antral aspergillosis are briefly discussed.
Paranasal sinus aspergillosis has usually been considered a rare disease, but it is seen more frequently in both immunocompromised and immunocompetent persons. Invasion may reach the sinuses via the nose or from the mouth after dental procedures. Even though the infection is usually limited to one or more sinuses, it may in certain cases extend to vascular or intracranial structures with a fatal outcome. In these cases, aggressive treatment is justified. We report a case of maxillary sinus aspergillosis that developed after dental extraction. Attention should be given to this possibility even after an apparently uncomplicated dental extraction.
We studied the histopathology and clinicopathologic correlates of invasive cavitary pulmonary aspergillosis in 11 immunosuppressed patients with disseminated malignancy. In most patients cavities were produced by separation of necrotic from viable lung, resulting in an intracavitary sequestrum ("lung ball"). Central dissolution of large necrotic areas and suppurative granulomatous aspergillary pneumonia were additional causes of cavities in three patients. In four patients with chronic cavities sequestra had been replaced by intracavitary mycetomas ("fungus balls"). Neutrophils usually were numerous at the interface of the sequestrum and adjacent lung, but were minimally present in three patients with prolonged severe neutropenia. The lack of neutrophils in some patients suggests that factors other than neutrophil-derived proteases may be important in cavity formation. A prominent giant cell reaction was seen in three patients with chronic cavities. Hemoptysis occurred in five patients and massive hemoptysis due to a bronchoarterial fistula caused the death of one patient. The "air-crescent" sign was not observed radiographically in any patient and is therefore considered to be an insensitive marker for lung cavitation in invasive aspergillosis. Persistent intracavitary fungal growth may serve as a reservoir for recurrent fungal invasion in patients with prolonged or repeated episodes of severe neutropenia.
Primary renal aspergillosis has been reported only five times previously. We report the first case with primary renal aspergillosis where reconstructive and not extirpative surgery was used. Patients who have predisposing factors such as diabetes, malignancies, or immunosuppression represent the primary target for fungal infection. In these patients the clinical picture of nonspecific and fungal pyelonephritis are similar. Therefore fungal infections should be considered in the differential diagnosis of urinary tract infections.
This is the first article of a familial occurrence of allergic bronchopulmonary aspergillosis in a father and daughter. Serologic studies revealed serum precipitins and elevated IgG or IgE antibody activity against certain Aspergillus species. Investigation of the home revealed an environmental source of exposure. Another family member demonstrated serum precipitins and an IgG antibody response to the isolated Aspergillus species without evidence of allergic bronchopulmonary aspergillosis.
A lung biopsy specimen was obtained from a 10-year-old boy with cystic fibrosis and allergic bronchopulmonary aspergillosis. Light microscopy revealed a marked inflammatory process that was largely bronchocentric. Infiltrating cells included lymphocytes, plasma cells, monocytes, and numerous eosinophils. Elastin layers were intact in blood vessels and markedly disrupted in bronchioles. By immunofluorescent, major basic protein was demonstrated in eosinophils, was freely deposited outside of eosinophils, especially in the interlobular septum, and was taken up by macrophages. A number of lymphocytes stained positively for IgE. Through an immunoperoxidase stain, septate hyphae of Aspergillus were clearly observed in the lung parenchyma. A significant increase in interleukin-2 positive-staining T cells was observed with an approximate 2:1 ratio of helper to suppressor cells. The use of newer immunohistologic techniques has enabled us to gain additional insights into the pathogenesis of allergic bronchopulmonary aspergillosis.
Individual immunoprint patterns of sodium dodecylsulfate-polyacrylamide gel electrophoresis-separated Aspergillus fumigatus (Af) allergens/antigens were evaluated in 28 patients with allergic bronchopulmonary aspergillosis in stages II to V. It could be demonstrated that active disease (stage III) is characterized by a very strong IgE response against a variety of Af components, whereas the IgE antibody pattern in corticosteroid-treated patients who have demonstrated improvement is much weaker. In patients in remission (stage II), it is minimal. In contrast, many patients in stage V without corticosteroid treatment demonstrated a strong reactivity of IgE antibodies, indicating persisting active disease. The pattern of IgG antibodies with individual Af components resembles, in general, that of IgE antibodies; however, discrimination between different stages and between treated patients is much weaker. Our results indicate that a certain relationship between the different stages of allergic bronchopulmonary aspergillosis and Af immunoprint patterns exists.
The clinicopathologic characteristics of invasive oral aspergillosis in 16 immunocompromised patients who developed this infection during antileukemic chemotherapy are described. The primary site of the infection was the marginal gingiva, there was severe spontaneous pain, and the patients developed spiking fever and granulocytopenia. Necrotic ulceration of the gingiva rapidly extended to the contiguous mucosa, muscle, and bone. Microscopically, the necrotic tissue contained thrombotic vascular infarcts and there were hyphae that showed frequent transverse septa and dichotomous branching. The invasive organisms were not responsive to amphotericin B in the absence of remission of the leukemia and restoration of the depressed host defenses. In 15 patients who showed improvement of hematologic status, oral aspergillosis was controlled by the combination of antifungal chemotherapy and debridement of necrotic tissues.
Aspergillosis of the central nervous system is rare. It most commonly occurs in patients with long-standing immunosuppression. To our knowledge this is the first reported case describing the magnetic resonance imaging (MRI) findings in cerebral aspergillosis. The computed tomography (CT) scan findings are also included.
BACKGROUND: Voriconazole is a novel triazole antifungal with a broad spectrum including Aspergillus species. We conducted an open, noncomparative multicenter study to evaluate the efficacy and safety of voriconazole in subacute invasive and chronic pulmonary aspergillosis (CPA). METHODS: Patients without profound neutropenia and a proven or probable diagnosis of subacute invasive aspergillosis (IA) or CPA received voriconazole 200 mg twice daily for a period of 4-24 weeks as primary or salvage therapy. Dose escalation was allowed if efficacy was suboptimal, and toleration and safety were satisfactory. Response was assessed by clinical, radiological and mycological changes. A complete or partial response in subacute IA and improved or stable in CPA were assessed as favorable responses. RESULTS: Of 39 patients treated, 36 were assessable. The majority of patients had subacute IA (n = 21), proven in all 11 extra-pulmonary and in 23/25 (92%) of the pulmonary cases. Voriconazole was given as primary therapy in 22 (61%). All patients receiving salvage therapy (n = 14) had refractory IA, having failed itraconazole or amphotericin B (AmB) or both. Overall, a complete or partial response was seen in 9/21(43%) of subacute IA and improved or stable in 12/15 (80%) of those with CPA. Adverse events, mainly liver function test abnormalities, skin reactions, and visual disturbances were mild and transient, leading to early discontinuation of treatment in 5 cases. CONCLUSIONS: In patients with subacute IA and CPA, voriconazole was efficacious as salvage or primary therapy.
The exposure to Aspergillus organisms/spores is likely common, but disease caused by tissue invasion with these fungi is uncommon and occurs primarily in the setting of immunosuppression. We report a case of rapidly advancing invasive endomyocardial aspergillosis secondary to prolonged usage of multiple broad-spectrum antibiotics in a nonimmunocompromised host. A 36-year-old cotton textile worker presented to our institution with a 3-month history of weight loss and fatigue. He reported receiving prolonged use of multiple broad-spectrum antibiotic treatment. The echocardiogram demonstrated multiple endomyocardial vegetations and a mass in the left atrium. Myocardial biopsy specimen revealed an invasive endomyocardial aspergillosis. The patient was investigated for immune deficiency including HIV, and this workup was negative. Treatment was started with amphotericin B and heparin for presumed left atrial thrombus. The patient died because of a rupture of mycotic aneurysm that resulted in cerebral hemorrhage. This case illustrates the risk of an invasive fungal infection in a nonimmunocompromised host who is a prolonged user of antibiotics in the setting of environmental exposure of opportunistic invasive fungal infections.
OBJECTIVE: Pulmonary sequestration (PS) is an uncommon congenital disease. Symptoms when present are usually secondary to pyogenic infection. Our objective was to draw attention on superimposed fungal infection. METHODS: During the last 20 years, we operated upon 19 intralobar PS. Four of six patients operated during the last decade proved to have intralobar PS containing Aspergillus. RESULTS: In one patient aspergillosis presented as an aspergilloma and communications between the sequestration and small bronchi were present. In another patient diagnosis was made before operation because of positive precipitins test. In two patients aspegillosis was discovered by the pathologist. CONCLUSIONS: Review of literature demonstrates PS fungal colonization to be a rare but recently reported entity (14 cases reported). The observation of four consecutive patients leads us to suggest that PS aspergillosis must be considered in order to evaluate its incidence.
A lot of in-house polymerase chain reaction assays have been reported for diagnosis of invasive aspergillosis and disseminated candidosis. Encouraging results have been published to anticipate the diagnosis over the conventional microbiological methods. However, the absence of standardized methods has led to diverging results. As a consequence, these tests are not recognized as consensual diagnostic criteria, in contrast with some antigenemia detection kits. The major breakthrough for improving the results of these methods is the emergence of real-time technologies. This markedly improves the reliability of the PCR results by dramatically decreasing the risk of false positive results due to PCR products carryover. Moreover, using the quantitative results provided by this technique, this allows to rapidly compare the efficiency of primers, probes, and DNA extraction methods. Therefore, the hope is to identify the more specific and sensitive parameters to implement comparative studies. Automated DNA extraction should also be useful to achieve this goal. Whatever sophisticated technology is used, we still have to define the meaning of detecting nucleic acids in a given clinical sample. This seems simple in normally sterile anatomical sites but less obvious for example in respiratory specimens for invasive aspergillosis or in blood for candidosis in heavily colonized patients. Additional studies of the kinetics of fungal DNA are needed. The development of real-time technology should improve our knowledge in order to give the clinicians informative clues for making a decision.